Practice Gap

Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition characterized by inflammatory nodules, abscesses, sinus tracts, fistulae, and scarring, mainly in intertriginous areas. The extent of disease—classified using the Hurley staging system (stages I–III)—helps guide treatment, which includes medical management and surgical intervention in later stages.

First-line treatment of HS includes topical or systemic medications, or both. Surgical therapy typically is reserved for refractory HS in moderate to severe disease (Hurley stages II and III) and is combined with pharmacotherapy. Specifically, clinical management guidelines issued by an expert committee of the United States and Canadian Hidradenitis Suppurativa Foundations recommend excision or deroofing for recurrent nodules and tunnels.¹

Surgical options for HS that are available to the outpatient dermatologist include incision and drainage, electrosurgery, CO₂ laser evaporation, excision, and deroofing (also known as unroofing).² Deroofing is a fairly novel therapy; many dermatologists are unfamiliar with the procedure. A PubMed search of articles indexed for MEDLINE related to HS prior to 2010 revealed only 1 article containing the word deroofing and only 4 articles containing unroofing.

The pathophysiology of HS has important implications for successful treatment. Inflammation of the follicular pilosebaceous unit along with follicular occlusion create challenges with treatment.³ It is postulated that a defect in the glassy membrane of the infra-infundibular wall predisposes the pilosebaceous follicle to lose its structural integrality as pressure builds from plugging of the duct,⁴ which can result in the clinical hallmarks of HS including tunneling tracts, bridging nodules, abscesses, and fistulae that form with lateral expansion of the plugged follicle.

Leaking of the contents of these plugged follicles into surrounding tissue produces an inflammatory response in characteristic HS lesions. Because debris within the lesions moves laterally instead of being able to burst to the surface, the lesions have difficulty fully healing. Unroofing the lesions and removing built-up debris allows them to heal more expediently and quiets the underlying immune response by removing the stimulus.⁴

Herein, we describe the benefits, risks, and surgical process of deroofing for HS.

Technique and Tools

Deroofing is performed under local anesthesia, stepwise as follows:

1. Identify sinus tracts and infiltrate the area with lidocaine (Figure, A).

2. Use a blunt probe to define the borders of the area to be unroofed and to evaluate for any communicating sinus tracts (Figure, B).

3. Remove the roof of underlying abscesses and tracts, using a probe as a guide (Figure, C).

4. Enter through the skin or sinus opening using electrocautery or with a scalpel or scissors; perform blunt dissection.

5. Reflect back the entirety of skin overlying the probed areas and remove the skin to expose the base of the lesion (Figure, D).

6. Explore the exposed base and walls of the lesion with the probe again to assess for hidden tracts; take care not to create false tracts.

7. Debride the surgical wound using curettage or rough gauze grattage to remove remaining inflammatory debris or biofilm. To achieve hemostasis, apply aluminum chloride or ferric chloride. Coat the wound with petroleum jelly and gauze and allow it to heal by secondary intention.

8. Educate the patient on wound care—once-daily gentle cleansing with soap and water, followed by application of a moist dressing—which is similar to wound healing by secondary intention from other causes.^2,4

Practice Implications

A deroofing procedure has many benefits compared to other surgical modalities for the treatment of HS. Deroofing requires only a probe, curette, and electrocautery device, making the procedure more cost-effective than excision, which requires a full tray of equipment and sutures. Furthermore, margins do not need to be taken with deroofing, and no undermining or closure is needed, which saves time during the operation and minimizes the risk for complications, including dehiscence and formation of new sinus tracts.⁴ No specialized equipment, such as a CO₂ laser, is required, which makes deroofing accessible to every clinical dermatologist in any demographic or geographic setting.

Evidence of Benefit—Saylor and colleagues⁵ found that deroofing carries a 12.5% complication rate, which includes postoperative bleeding, hypergranulation tissue, and rarely wound infection. This rate is significantly lower than the 26% complication rate associated with local excision, which includes wound dehiscence, infection, and contracture (P<.001). Deroofing also was found to have an HS recurrence rate of 14.5%, which is significantly less than the 30% recurrence rate seen with local excision (P=.015). Saylor et al⁵ also concluded that incision and drainage was recommended only for immediate relief of HS because of its 100% recurrence rate.

van der Zee² reported on 88 lesions from 44 patients that were treated by surgical deroofing, resulting in an average defect of 3.0 cm in length and a mean healing time of 14 days. The typical outcome was cosmetically acceptable scarring; this finding was supported by a postoperative survey (>1 year), to which 37 of 44 patients responded and assigned an average satisfaction score of 8 (of a possible 10) and a recommendation rate of 90%.²

Procedural Coding—Specific Current Procedural Terminology codes (11450-11471) from the International Classification of Diseases, Tenth Revision, exist for HS deroofing procedures; the applicable code for a given case depends on the final length of the surgical defect. Documentation to support these codes is similar to the note for an excision procedure, taking care to include location, depth, and length of the excision; healing by secondary intention; and the diagnosis of HS.

Final Thoughts

Deroofing is a surgical option that can be beneficial to patients with HS. It is a relatively simple procedure available to any dermatologist, regardless of setting. We encourage dermatologists to consider deroofing, even in patients with Hurley stage II lesions, because it can yield cosmetically acceptable and definitive results, given the variety of therapies available for HS. Deroofing also can be superior to standard excision, especially because of the potential complications with standard excision and quicker operative time with deroofing. As more providers become familiar with the deroofing procedure for HS, further studies can be undertaken to add to the paucity of data about deroofing and how it compares to other surgical treatments.

Practice Gap

Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition characterized by inflammatory nodules, abscesses, sinus tracts, fistulae, and scarring, mainly in intertriginous areas. The extent of disease—classified using the Hurley staging system (stages I–III)—helps guide treatment, which includes medical management and surgical intervention in later stages.

First-line treatment of HS includes topical or systemic medications, or both. Surgical therapy typically is reserved for refractory HS in moderate to severe disease (Hurley stages II and III) and is combined with pharmacotherapy. Specifically, clinical management guidelines issued by an expert committee of the United States and Canadian Hidradenitis Suppurativa Foundations recommend excision or deroofing for recurrent nodules and tunnels.¹

Surgical options for HS that are available to the outpatient dermatologist include incision and drainage, electrosurgery, CO₂ laser evaporation, excision, and deroofing (also known as unroofing).² Deroofing is a fairly novel therapy; many dermatologists are unfamiliar with the procedure. A PubMed search of articles indexed for MEDLINE related to HS prior to 2010 revealed only 1 article containing the word deroofing and only 4 articles containing unroofing.

The pathophysiology of HS has important implications for successful treatment. Inflammation of the follicular pilosebaceous unit along with follicular occlusion create challenges with treatment.³ It is postulated that a defect in the glassy membrane of the infra-infundibular wall predisposes the pilosebaceous follicle to lose its structural integrality as pressure builds from plugging of the duct,⁴ which can result in the clinical hallmarks of HS including tunneling tracts, bridging nodules, abscesses, and fistulae that form with lateral expansion of the plugged follicle.

Leaking of the contents of these plugged follicles into surrounding tissue produces an inflammatory response in characteristic HS lesions. Because debris within the lesions moves laterally instead of being able to burst to the surface, the lesions have difficulty fully healing. Unroofing the lesions and removing built-up debris allows them to heal more expediently and quiets the underlying immune response by removing the stimulus.⁴

Herein, we describe the benefits, risks, and surgical process of deroofing for HS.

Technique and Tools

Deroofing is performed under local anesthesia, stepwise as follows:

1. Identify sinus tracts and infiltrate the area with lidocaine (Figure, A).

2. Use a blunt probe to define the borders of the area to be unroofed and to evaluate for any communicating sinus tracts (Figure, B).

3. Remove the roof of underlying abscesses and tracts, using a probe as a guide (Figure, C).

4. Enter through the skin or sinus opening using electrocautery or with a scalpel or scissors; perform blunt dissection.

5. Reflect back the entirety of skin overlying the probed areas and remove the skin to expose the base of the lesion (Figure, D).

6. Explore the exposed base and walls of the lesion with the probe again to assess for hidden tracts; take care not to create false tracts.

7. Debride the surgical wound using curettage or rough gauze grattage to remove remaining inflammatory debris or biofilm. To achieve hemostasis, apply aluminum chloride or ferric chloride. Coat the wound with petroleum jelly and gauze and allow it to heal by secondary intention.

8. Educate the patient on wound care—once-daily gentle cleansing with soap and water, followed by application of a moist dressing—which is similar to wound healing by secondary intention from other causes.^2,4

Practice Implications

A deroofing procedure has many benefits compared to other surgical modalities for the treatment of HS. Deroofing requires only a probe, curette, and electrocautery device, making the procedure more cost-effective than excision, which requires a full tray of equipment and sutures. Furthermore, margins do not need to be taken with deroofing, and no undermining or closure is needed, which saves time during the operation and minimizes the risk for complications, including dehiscence and formation of new sinus tracts.⁴ No specialized equipment, such as a CO₂ laser, is required, which makes deroofing accessible to every clinical dermatologist in any demographic or geographic setting.

Evidence of Benefit—Saylor and colleagues⁵ found that deroofing carries a 12.5% complication rate, which includes postoperative bleeding, hypergranulation tissue, and rarely wound infection. This rate is significantly lower than the 26% complication rate associated with local excision, which includes wound dehiscence, infection, and contracture (P<.001). Deroofing also was found to have an HS recurrence rate of 14.5%, which is significantly less than the 30% recurrence rate seen with local excision (P=.015). Saylor et al⁵ also concluded that incision and drainage was recommended only for immediate relief of HS because of its 100% recurrence rate.

van der Zee² reported on 88 lesions from 44 patients that were treated by surgical deroofing, resulting in an average defect of 3.0 cm in length and a mean healing time of 14 days. The typical outcome was cosmetically acceptable scarring; this finding was supported by a postoperative survey (>1 year), to which 37 of 44 patients responded and assigned an average satisfaction score of 8 (of a possible 10) and a recommendation rate of 90%.²

Procedural Coding—Specific Current Procedural Terminology codes (11450-11471) from the International Classification of Diseases, Tenth Revision, exist for HS deroofing procedures; the applicable code for a given case depends on the final length of the surgical defect. Documentation to support these codes is similar to the note for an excision procedure, taking care to include location, depth, and length of the excision; healing by secondary intention; and the diagnosis of HS.

Final Thoughts

Deroofing is a surgical option that can be beneficial to patients with HS. It is a relatively simple procedure available to any dermatologist, regardless of setting. We encourage dermatologists to consider deroofing, even in patients with Hurley stage II lesions, because it can yield cosmetically acceptable and definitive results, given the variety of therapies available for HS. Deroofing also can be superior to standard excision, especially because of the potential complications with standard excision and quicker operative time with deroofing. As more providers become familiar with the deroofing procedure for HS, further studies can be undertaken to add to the paucity of data about deroofing and how it compares to other surgical treatments.

Practice Gap

Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition characterized by inflammatory nodules, abscesses, sinus tracts, fistulae, and scarring, mainly in intertriginous areas. The extent of disease—classified using the Hurley staging system (stages I–III)—helps guide treatment, which includes medical management and surgical intervention in later stages.

First-line treatment of HS includes topical or systemic medications, or both. Surgical therapy typically is reserved for refractory HS in moderate to severe disease (Hurley stages II and III) and is combined with pharmacotherapy. Specifically, clinical management guidelines issued by an expert committee of the United States and Canadian Hidradenitis Suppurativa Foundations recommend excision or deroofing for recurrent nodules and tunnels.¹

Surgical options for HS that are available to the outpatient dermatologist include incision and drainage, electrosurgery, CO₂ laser evaporation, excision, and deroofing (also known as unroofing).² Deroofing is a fairly novel therapy; many dermatologists are unfamiliar with the procedure. A PubMed search of articles indexed for MEDLINE related to HS prior to 2010 revealed only 1 article containing the word deroofing and only 4 articles containing unroofing.

The pathophysiology of HS has important implications for successful treatment. Inflammation of the follicular pilosebaceous unit along with follicular occlusion create challenges with treatment.³ It is postulated that a defect in the glassy membrane of the infra-infundibular wall predisposes the pilosebaceous follicle to lose its structural integrality as pressure builds from plugging of the duct,⁴ which can result in the clinical hallmarks of HS including tunneling tracts, bridging nodules, abscesses, and fistulae that form with lateral expansion of the plugged follicle.

Leaking of the contents of these plugged follicles into surrounding tissue produces an inflammatory response in characteristic HS lesions. Because debris within the lesions moves laterally instead of being able to burst to the surface, the lesions have difficulty fully healing. Unroofing the lesions and removing built-up debris allows them to heal more expediently and quiets the underlying immune response by removing the stimulus.⁴

Herein, we describe the benefits, risks, and surgical process of deroofing for HS.

Technique and Tools

Deroofing is performed under local anesthesia, stepwise as follows:

1. Identify sinus tracts and infiltrate the area with lidocaine (Figure, A).

2. Use a blunt probe to define the borders of the area to be unroofed and to evaluate for any communicating sinus tracts (Figure, B).

3. Remove the roof of underlying abscesses and tracts, using a probe as a guide (Figure, C).

4. Enter through the skin or sinus opening using electrocautery or with a scalpel or scissors; perform blunt dissection.

5. Reflect back the entirety of skin overlying the probed areas and remove the skin to expose the base of the lesion (Figure, D).

6. Explore the exposed base and walls of the lesion with the probe again to assess for hidden tracts; take care not to create false tracts.

7. Debride the surgical wound using curettage or rough gauze grattage to remove remaining inflammatory debris or biofilm. To achieve hemostasis, apply aluminum chloride or ferric chloride. Coat the wound with petroleum jelly and gauze and allow it to heal by secondary intention.

8. Educate the patient on wound care—once-daily gentle cleansing with soap and water, followed by application of a moist dressing—which is similar to wound healing by secondary intention from other causes.^2,4

Practice Implications

A deroofing procedure has many benefits compared to other surgical modalities for the treatment of HS. Deroofing requires only a probe, curette, and electrocautery device, making the procedure more cost-effective than excision, which requires a full tray of equipment and sutures. Furthermore, margins do not need to be taken with deroofing, and no undermining or closure is needed, which saves time during the operation and minimizes the risk for complications, including dehiscence and formation of new sinus tracts.⁴ No specialized equipment, such as a CO₂ laser, is required, which makes deroofing accessible to every clinical dermatologist in any demographic or geographic setting.

Evidence of Benefit—Saylor and colleagues⁵ found that deroofing carries a 12.5% complication rate, which includes postoperative bleeding, hypergranulation tissue, and rarely wound infection. This rate is significantly lower than the 26% complication rate associated with local excision, which includes wound dehiscence, infection, and contracture (P<.001). Deroofing also was found to have an HS recurrence rate of 14.5%, which is significantly less than the 30% recurrence rate seen with local excision (P=.015). Saylor et al⁵ also concluded that incision and drainage was recommended only for immediate relief of HS because of its 100% recurrence rate.

van der Zee² reported on 88 lesions from 44 patients that were treated by surgical deroofing, resulting in an average defect of 3.0 cm in length and a mean healing time of 14 days. The typical outcome was cosmetically acceptable scarring; this finding was supported by a postoperative survey (>1 year), to which 37 of 44 patients responded and assigned an average satisfaction score of 8 (of a possible 10) and a recommendation rate of 90%.²

Procedural Coding—Specific Current Procedural Terminology codes (11450-11471) from the International Classification of Diseases, Tenth Revision, exist for HS deroofing procedures; the applicable code for a given case depends on the final length of the surgical defect. Documentation to support these codes is similar to the note for an excision procedure, taking care to include location, depth, and length of the excision; healing by secondary intention; and the diagnosis of HS.

Final Thoughts

Deroofing is a surgical option that can be beneficial to patients with HS. It is a relatively simple procedure available to any dermatologist, regardless of setting. We encourage dermatologists to consider deroofing, even in patients with Hurley stage II lesions, because it can yield cosmetically acceptable and definitive results, given the variety of therapies available for HS. Deroofing also can be superior to standard excision, especially because of the potential complications with standard excision and quicker operative time with deroofing. As more providers become familiar with the deroofing procedure for HS, further studies can be undertaken to add to the paucity of data about deroofing and how it compares to other surgical treatments.

GHENT, BELGIUM – A strong numerical signal suggests the addition of a selective cyclooxygenase-2 (COX-2) inhibitor to a tumor necrosis factor (TNF) inhibitor can reduce spinal radiographic progression in patients with active radiographic axial spondyloarthritis (axSpA) over 2 years, although results are not statistically significant.

Becky McCall/MDedge News

Lead researcher and rheumatologist, Fabian Proft, MD, based at Charité University Medicine, Berlin, presented the findings of the study at the 13th International Congress on Spondyloarthritides.

Only 97 patients completed the study, and its follow-up period lasted 2 years, which is a relatively short period of time in which to determine the effects of an intervention that might affect structural progression of the spine, Dr. Proft said.

“Based on these data, I won’t treat all my patients with celecoxib,” he told this news organization. However, he added that, “If I have a patient with residual symptoms under biological DMARDs [disease-modifying antirheumatic drugs], and I feel they are at high risk of radiographic spinal progression and they still have symptoms, then I would add in an NSAID – and for that I’d choose a selective COX-2 inhibitor based on radiographic spinal progression data.”

Walter P. Maksymowych, MD, rheumatologist from the University of Alberta, Calgary, commented on the study findings in an interview. “This is an important clinical question because we want to know whether we should be adding an anti-inflammatory in patients who are on biologic therapies. There’s been a long debate and investigation into whether anti-inflammatories might prevent new bone formation and thereby prevent disease progression.”

He went on by acknowledging that there was no statistically significant difference in the primary endpoint (change in modified Stoke Ankylosing Spondylitis Spinal Score [mSASSS]) between the groups, but added that, “there was a sizable numerical difference, and I think this leaves the community somewhat hanging dry without a definitive answer. However, I do have concerns about whether there was an adequate sample size to address the study question.”
 

To add or not to add a selective COX-2 inhibitor to TNF inhibitor in axSpA treatment

The study aimed to investigate the effect of a selective COX-2 inhibitor when added to anti-TNF therapy with golimumab (Simponi), compared with golimumab therapy alone, on the progression of spinal structural damage over 2 years in patients with active radiographic axSpA.

“To date, we don’t have many treatments with evidence of reducing spinal radiographic progression in axSpA,” Dr. Proft said. “There was one study showing an effect of celecoxib, but another with diclofenac that failed to show any effect. As a result, there was a hypothesis that perhaps there was a selective COX-2 inhibitor effect.”

To investigate this further, Dr. Proft selected patients with high radiographic axSpA disease activity (Bath Ankylosing Spondylitis Disease Activity Index [BASDAI] ≥ 4) and with existing structural changes – both recognized risk factors for further progression. Participants had to have either an elevated C-reactive protein (CRP) > 5 mg/L and/or ≥ 1 syndesmophyte at screening, as well as a history of inadequate response to at least two DMARDs. Other patient risk factors for radiographic spinal progression included male gender and smoking. Duration of axSpA was unlimited.

Three radiographic readers were blinded for all clinical data and chronology. The primary endpoint was the change in mSASSS, while secondary endpoints were the presence of new syndesmophytes and clinical outcomes including activity, function, mobility, and health-related quality of life, as well as safety assessments.

Patients were treated with only golimumab (50 mg subcutaneous every 4 weeks) for the first 12 weeks and then only those patients with a good clinical response (n = 109) went into phase two of the study, at which point they were randomized 1:1 to golimumab monotherapy (control, 50 mg subcutaneous every 4 weeks), or golimumab (50 mg subcutaneous every 4 weeks) plus celecoxib (400 mg once daily) for 2 years. Radiographs were taken at baseline (week 0) and after 2 years. A total of 45 patients completed the combination therapy and 52 completed the monotherapy.
 

No statistical significance but a numerical difference found

“The primary outcome, which was change in mSASSS score, clearly shows a numerical difference between the combination arm at 1.1 and the monotherapy arm at 1.7 points, showing more structural progression in the monotherapy arm, compared to the combination arm,” Dr. Proft reported. However, he stressed that this difference did not reach statistical significance.

New syndesmophytes occurred in 25% with monotherapy and 11.1% with combination treatment. Again, this difference did not reach statistical significance.

“This might be due to sample size but also to the length of follow-up because a longer follow-up [given structural changes occur relatively slowly] might have shown a greater difference,” Dr. Proft pointed out.

Clinical data, according to Ankylosing Spondylitis Disease Activity Score with CRP and BASDAI, showed that both groups responded very well to therapy, and there were no differences seen between the two groups in terms of clinical parameters.

“It is important when we add a drug – and we know that NSAIDs can have safety concerns – that we do not see any statistically significant serious adverse events between patient groups,” Dr. Proft noted.

There were no significant differences in adverse events between monotherapy and combination therapy. There were 162 infections in the combination arm and 150 in the monotherapy arm. Combination therapy led to seven serious adverse events, and monotherapy occurred with five adverse events.

Dr. Proft added that four patients discontinued in the combination arm, compared with only one in the monotherapy arm, with a variety of different reasons for the discontinuations.

The study was supported by a grant from the German Ministry of Education and Research, and golimumab was provided free of charge by Merck Sharp & Dohme. Dr. Proft reported serving on speakers bureaus for Amgen, AbbVie, Bristol-Myers Squibb, Celgene, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, Roche, and UCB; serving as a consultant to Novartis; and receiving grant or research support from Novartis, UCB, and Lilly. Dr. Maksymowych declared having no relevant conflicts of interest.

GHENT, BELGIUM – A strong numerical signal suggests the addition of a selective cyclooxygenase-2 (COX-2) inhibitor to a tumor necrosis factor (TNF) inhibitor can reduce spinal radiographic progression in patients with active radiographic axial spondyloarthritis (axSpA) over 2 years, although results are not statistically significant.

Becky McCall/MDedge News

Lead researcher and rheumatologist, Fabian Proft, MD, based at Charité University Medicine, Berlin, presented the findings of the study at the 13th International Congress on Spondyloarthritides.

Only 97 patients completed the study, and its follow-up period lasted 2 years, which is a relatively short period of time in which to determine the effects of an intervention that might affect structural progression of the spine, Dr. Proft said.

“Based on these data, I won’t treat all my patients with celecoxib,” he told this news organization. However, he added that, “If I have a patient with residual symptoms under biological DMARDs [disease-modifying antirheumatic drugs], and I feel they are at high risk of radiographic spinal progression and they still have symptoms, then I would add in an NSAID – and for that I’d choose a selective COX-2 inhibitor based on radiographic spinal progression data.”

Walter P. Maksymowych, MD, rheumatologist from the University of Alberta, Calgary, commented on the study findings in an interview. “This is an important clinical question because we want to know whether we should be adding an anti-inflammatory in patients who are on biologic therapies. There’s been a long debate and investigation into whether anti-inflammatories might prevent new bone formation and thereby prevent disease progression.”

He went on by acknowledging that there was no statistically significant difference in the primary endpoint (change in modified Stoke Ankylosing Spondylitis Spinal Score [mSASSS]) between the groups, but added that, “there was a sizable numerical difference, and I think this leaves the community somewhat hanging dry without a definitive answer. However, I do have concerns about whether there was an adequate sample size to address the study question.”
 

To add or not to add a selective COX-2 inhibitor to TNF inhibitor in axSpA treatment

The study aimed to investigate the effect of a selective COX-2 inhibitor when added to anti-TNF therapy with golimumab (Simponi), compared with golimumab therapy alone, on the progression of spinal structural damage over 2 years in patients with active radiographic axSpA.

“To date, we don’t have many treatments with evidence of reducing spinal radiographic progression in axSpA,” Dr. Proft said. “There was one study showing an effect of celecoxib, but another with diclofenac that failed to show any effect. As a result, there was a hypothesis that perhaps there was a selective COX-2 inhibitor effect.”

To investigate this further, Dr. Proft selected patients with high radiographic axSpA disease activity (Bath Ankylosing Spondylitis Disease Activity Index [BASDAI] ≥ 4) and with existing structural changes – both recognized risk factors for further progression. Participants had to have either an elevated C-reactive protein (CRP) > 5 mg/L and/or ≥ 1 syndesmophyte at screening, as well as a history of inadequate response to at least two DMARDs. Other patient risk factors for radiographic spinal progression included male gender and smoking. Duration of axSpA was unlimited.

Three radiographic readers were blinded for all clinical data and chronology. The primary endpoint was the change in mSASSS, while secondary endpoints were the presence of new syndesmophytes and clinical outcomes including activity, function, mobility, and health-related quality of life, as well as safety assessments.

Patients were treated with only golimumab (50 mg subcutaneous every 4 weeks) for the first 12 weeks and then only those patients with a good clinical response (n = 109) went into phase two of the study, at which point they were randomized 1:1 to golimumab monotherapy (control, 50 mg subcutaneous every 4 weeks), or golimumab (50 mg subcutaneous every 4 weeks) plus celecoxib (400 mg once daily) for 2 years. Radiographs were taken at baseline (week 0) and after 2 years. A total of 45 patients completed the combination therapy and 52 completed the monotherapy.
 

No statistical significance but a numerical difference found

“The primary outcome, which was change in mSASSS score, clearly shows a numerical difference between the combination arm at 1.1 and the monotherapy arm at 1.7 points, showing more structural progression in the monotherapy arm, compared to the combination arm,” Dr. Proft reported. However, he stressed that this difference did not reach statistical significance.

New syndesmophytes occurred in 25% with monotherapy and 11.1% with combination treatment. Again, this difference did not reach statistical significance.

“This might be due to sample size but also to the length of follow-up because a longer follow-up [given structural changes occur relatively slowly] might have shown a greater difference,” Dr. Proft pointed out.

Clinical data, according to Ankylosing Spondylitis Disease Activity Score with CRP and BASDAI, showed that both groups responded very well to therapy, and there were no differences seen between the two groups in terms of clinical parameters.

“It is important when we add a drug – and we know that NSAIDs can have safety concerns – that we do not see any statistically significant serious adverse events between patient groups,” Dr. Proft noted.

There were no significant differences in adverse events between monotherapy and combination therapy. There were 162 infections in the combination arm and 150 in the monotherapy arm. Combination therapy led to seven serious adverse events, and monotherapy occurred with five adverse events.

Dr. Proft added that four patients discontinued in the combination arm, compared with only one in the monotherapy arm, with a variety of different reasons for the discontinuations.

The study was supported by a grant from the German Ministry of Education and Research, and golimumab was provided free of charge by Merck Sharp & Dohme. Dr. Proft reported serving on speakers bureaus for Amgen, AbbVie, Bristol-Myers Squibb, Celgene, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, Roche, and UCB; serving as a consultant to Novartis; and receiving grant or research support from Novartis, UCB, and Lilly. Dr. Maksymowych declared having no relevant conflicts of interest.

GHENT, BELGIUM – A strong numerical signal suggests the addition of a selective cyclooxygenase-2 (COX-2) inhibitor to a tumor necrosis factor (TNF) inhibitor can reduce spinal radiographic progression in patients with active radiographic axial spondyloarthritis (axSpA) over 2 years, although results are not statistically significant.

Becky McCall/MDedge News

Lead researcher and rheumatologist, Fabian Proft, MD, based at Charité University Medicine, Berlin, presented the findings of the study at the 13th International Congress on Spondyloarthritides.

Only 97 patients completed the study, and its follow-up period lasted 2 years, which is a relatively short period of time in which to determine the effects of an intervention that might affect structural progression of the spine, Dr. Proft said.

“Based on these data, I won’t treat all my patients with celecoxib,” he told this news organization. However, he added that, “If I have a patient with residual symptoms under biological DMARDs [disease-modifying antirheumatic drugs], and I feel they are at high risk of radiographic spinal progression and they still have symptoms, then I would add in an NSAID – and for that I’d choose a selective COX-2 inhibitor based on radiographic spinal progression data.”

Walter P. Maksymowych, MD, rheumatologist from the University of Alberta, Calgary, commented on the study findings in an interview. “This is an important clinical question because we want to know whether we should be adding an anti-inflammatory in patients who are on biologic therapies. There’s been a long debate and investigation into whether anti-inflammatories might prevent new bone formation and thereby prevent disease progression.”

He went on by acknowledging that there was no statistically significant difference in the primary endpoint (change in modified Stoke Ankylosing Spondylitis Spinal Score [mSASSS]) between the groups, but added that, “there was a sizable numerical difference, and I think this leaves the community somewhat hanging dry without a definitive answer. However, I do have concerns about whether there was an adequate sample size to address the study question.”
 

To add or not to add a selective COX-2 inhibitor to TNF inhibitor in axSpA treatment

The study aimed to investigate the effect of a selective COX-2 inhibitor when added to anti-TNF therapy with golimumab (Simponi), compared with golimumab therapy alone, on the progression of spinal structural damage over 2 years in patients with active radiographic axSpA.

“To date, we don’t have many treatments with evidence of reducing spinal radiographic progression in axSpA,” Dr. Proft said. “There was one study showing an effect of celecoxib, but another with diclofenac that failed to show any effect. As a result, there was a hypothesis that perhaps there was a selective COX-2 inhibitor effect.”

To investigate this further, Dr. Proft selected patients with high radiographic axSpA disease activity (Bath Ankylosing Spondylitis Disease Activity Index [BASDAI] ≥ 4) and with existing structural changes – both recognized risk factors for further progression. Participants had to have either an elevated C-reactive protein (CRP) > 5 mg/L and/or ≥ 1 syndesmophyte at screening, as well as a history of inadequate response to at least two DMARDs. Other patient risk factors for radiographic spinal progression included male gender and smoking. Duration of axSpA was unlimited.

Three radiographic readers were blinded for all clinical data and chronology. The primary endpoint was the change in mSASSS, while secondary endpoints were the presence of new syndesmophytes and clinical outcomes including activity, function, mobility, and health-related quality of life, as well as safety assessments.

Patients were treated with only golimumab (50 mg subcutaneous every 4 weeks) for the first 12 weeks and then only those patients with a good clinical response (n = 109) went into phase two of the study, at which point they were randomized 1:1 to golimumab monotherapy (control, 50 mg subcutaneous every 4 weeks), or golimumab (50 mg subcutaneous every 4 weeks) plus celecoxib (400 mg once daily) for 2 years. Radiographs were taken at baseline (week 0) and after 2 years. A total of 45 patients completed the combination therapy and 52 completed the monotherapy.
 

No statistical significance but a numerical difference found

“The primary outcome, which was change in mSASSS score, clearly shows a numerical difference between the combination arm at 1.1 and the monotherapy arm at 1.7 points, showing more structural progression in the monotherapy arm, compared to the combination arm,” Dr. Proft reported. However, he stressed that this difference did not reach statistical significance.

New syndesmophytes occurred in 25% with monotherapy and 11.1% with combination treatment. Again, this difference did not reach statistical significance.

“This might be due to sample size but also to the length of follow-up because a longer follow-up [given structural changes occur relatively slowly] might have shown a greater difference,” Dr. Proft pointed out.

Clinical data, according to Ankylosing Spondylitis Disease Activity Score with CRP and BASDAI, showed that both groups responded very well to therapy, and there were no differences seen between the two groups in terms of clinical parameters.

“It is important when we add a drug – and we know that NSAIDs can have safety concerns – that we do not see any statistically significant serious adverse events between patient groups,” Dr. Proft noted.

There were no significant differences in adverse events between monotherapy and combination therapy. There were 162 infections in the combination arm and 150 in the monotherapy arm. Combination therapy led to seven serious adverse events, and monotherapy occurred with five adverse events.

Dr. Proft added that four patients discontinued in the combination arm, compared with only one in the monotherapy arm, with a variety of different reasons for the discontinuations.

The study was supported by a grant from the German Ministry of Education and Research, and golimumab was provided free of charge by Merck Sharp & Dohme. Dr. Proft reported serving on speakers bureaus for Amgen, AbbVie, Bristol-Myers Squibb, Celgene, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, Roche, and UCB; serving as a consultant to Novartis; and receiving grant or research support from Novartis, UCB, and Lilly. Dr. Maksymowych declared having no relevant conflicts of interest.

MILAN – Application of topical or both topical and oral polypodium leucotomos extract (PLE) was associated with significant reversal of adverse skin changes in patients with severe actinic keratoses (AKs) treated over 12 months, in a randomized, blinded study presented at the annual congress of the European Academy of Dermatology and Venereology.

At 12 months, the percentage of patients with a normal or almost normal honeycomb pattern when evaluated blindly with reflectance confocal microscopy (RCM) was about twice as great in either of the two groups that received PLE relative to those treated with topical photoprotection alone, according to Giovanni Pellacani, MD, PhD, chair of dermatology, University of Sapienza, Rome.

“In patients with severe actinic keratosis, the 12-month use of a PLE-based topical or oral photoprotection is associated with positive clinical and anatomical outcomes,” Dr. Pellacani said.

PLE, which is already commonly used in sun protection products, is derived from a South American species of fern and has been proposed for a broad array of dermatologic diseases. According to Dr. Pellacani, in vivo studies associating PLE with immune photoprotection make this agent particularly promising for severe AKs.

In this study involving two clinical research centers in Italy, 131 patients with photoaging and at least three AKs were randomized to one of three treatment arms. The control arm received topical photoprotection with an SPF of 100 or higher applied twice daily to all sun-exposed areas. The two treatment arms received the same topical photoprotection plus either a PLE-containing topical cream alone or a PLE-containing topical cream plus PLE in an oral form (240 mg) once daily

Patients were evaluated at 3 months, 6 months, and 1 year with several measures, including the Actinic Keratosis Area Score Index (AKASI) and the AK Field Assessment Scale Area (AK-FAS). They were also assessed with RCM. All clinical assessments and RCM evaluations, which assessed seven different parameters, such as honeycomb pattern, mottled pigmentation, and reticulated collagen, were performed by dermatologists blinded to the treatment assignment.

Complete data were available for 116 patients who completed all three evaluations over the 12 months of follow-up. On RCM, 50% of those receiving the oral and topical forms of PLE and 45% of those receiving topical PLE had normalization of the honeycomb pattern. These responses were significantly greater (P = .04 for both) than the 26% with normalization in the control group.

Although there were no significant differences in any of the other parameters evaluated by RCM, the improvement in the honeycomb pattern was accompanied by a 7% improvement in the AKASI score in patients taking PLE, either topically or orally and topically, while there was a 6% worsening (P < .001) among controls.

The AK-FAS score improved at 12 months by 26% in the group on oral/topical PLE and by 4% in the group on topical PLE. The score worsened by 13% among controls.

Over the course of the study, patients were permitted to take an appropriate therapy, such as imiquimod, cryotherapy, or 5-flourouracil if there was worsening of the AK-FAS score or if new lesions appeared.

On this measure, 38% of controls and 11% of those randomized to topical PLE had progressive disease versus only 2% of those randomized to take both topical and oral PLE, Dr. Pellacani reported.

The lower rate of new lesions or a start of a new drug over the course of the study in the group receiving both the topical and the oral formulations of PLE relative to those receiving topical PLE alone did not reach statistical significance, but Dr. Pellacani concluded that the addition of PLE to topical photoprotection without PLE seemed to provide a potentially clinically meaningful advantage.

Larger studies and longer term studies are needed, according to Dr. Pellacani, who noted that the substantial body of clinical studies associating PLE with benefit in a variety of dermatologic disorders has been weakened by the absence of well-designed studies that are adequately powered to guide clinical use.

Salvador González, MD, PhD, a dermatology specialist at Alcalá University, Madrid, also believes that PLE deserves further evaluation not just for photoprotection but for reinvigorating damaged skin due to its antioxidant and anti-inflammatory properties. He was the senior author of a 2020 paper in Photochemical and Photobiological Sciences that summarized the potential benefits of PLE in preventing damage related to sun exposure.

Among its mechanism, PLE generates reactive oxygen species (ROS) and prevents depletion of Langerhans cells induced by ultraviolet (UV) light, Dr. González explained in an interview. “At the cellular level, PLE activates tumor suppression p53, inhibits UV-induced COX-2 expression, reduces inflammation, and preventions immunosuppression,” he continued. In addition, he said PLE also prevents UV-A-induced common deletions related to mitochondrial damage and MMP1 expression induced by various UV wavelengths. 
“These molecular and cellular effects may translate into long-term inhibition of carcinogenesis including actinic keratosis,” he said, noting that all of these findings “justify the work by Pellacani and collaborators.”

Dr. Pellacani reports no potential conflicts of interest. Dr. González has a financial relationship with Cantabria Laboratories.

MILAN – Application of topical or both topical and oral polypodium leucotomos extract (PLE) was associated with significant reversal of adverse skin changes in patients with severe actinic keratoses (AKs) treated over 12 months, in a randomized, blinded study presented at the annual congress of the European Academy of Dermatology and Venereology.

At 12 months, the percentage of patients with a normal or almost normal honeycomb pattern when evaluated blindly with reflectance confocal microscopy (RCM) was about twice as great in either of the two groups that received PLE relative to those treated with topical photoprotection alone, according to Giovanni Pellacani, MD, PhD, chair of dermatology, University of Sapienza, Rome.

“In patients with severe actinic keratosis, the 12-month use of a PLE-based topical or oral photoprotection is associated with positive clinical and anatomical outcomes,” Dr. Pellacani said.

PLE, which is already commonly used in sun protection products, is derived from a South American species of fern and has been proposed for a broad array of dermatologic diseases. According to Dr. Pellacani, in vivo studies associating PLE with immune photoprotection make this agent particularly promising for severe AKs.

In this study involving two clinical research centers in Italy, 131 patients with photoaging and at least three AKs were randomized to one of three treatment arms. The control arm received topical photoprotection with an SPF of 100 or higher applied twice daily to all sun-exposed areas. The two treatment arms received the same topical photoprotection plus either a PLE-containing topical cream alone or a PLE-containing topical cream plus PLE in an oral form (240 mg) once daily

Patients were evaluated at 3 months, 6 months, and 1 year with several measures, including the Actinic Keratosis Area Score Index (AKASI) and the AK Field Assessment Scale Area (AK-FAS). They were also assessed with RCM. All clinical assessments and RCM evaluations, which assessed seven different parameters, such as honeycomb pattern, mottled pigmentation, and reticulated collagen, were performed by dermatologists blinded to the treatment assignment.

Complete data were available for 116 patients who completed all three evaluations over the 12 months of follow-up. On RCM, 50% of those receiving the oral and topical forms of PLE and 45% of those receiving topical PLE had normalization of the honeycomb pattern. These responses were significantly greater (P = .04 for both) than the 26% with normalization in the control group.

Although there were no significant differences in any of the other parameters evaluated by RCM, the improvement in the honeycomb pattern was accompanied by a 7% improvement in the AKASI score in patients taking PLE, either topically or orally and topically, while there was a 6% worsening (P < .001) among controls.

The AK-FAS score improved at 12 months by 26% in the group on oral/topical PLE and by 4% in the group on topical PLE. The score worsened by 13% among controls.

Over the course of the study, patients were permitted to take an appropriate therapy, such as imiquimod, cryotherapy, or 5-flourouracil if there was worsening of the AK-FAS score or if new lesions appeared.

On this measure, 38% of controls and 11% of those randomized to topical PLE had progressive disease versus only 2% of those randomized to take both topical and oral PLE, Dr. Pellacani reported.

The lower rate of new lesions or a start of a new drug over the course of the study in the group receiving both the topical and the oral formulations of PLE relative to those receiving topical PLE alone did not reach statistical significance, but Dr. Pellacani concluded that the addition of PLE to topical photoprotection without PLE seemed to provide a potentially clinically meaningful advantage.

Larger studies and longer term studies are needed, according to Dr. Pellacani, who noted that the substantial body of clinical studies associating PLE with benefit in a variety of dermatologic disorders has been weakened by the absence of well-designed studies that are adequately powered to guide clinical use.

Salvador González, MD, PhD, a dermatology specialist at Alcalá University, Madrid, also believes that PLE deserves further evaluation not just for photoprotection but for reinvigorating damaged skin due to its antioxidant and anti-inflammatory properties. He was the senior author of a 2020 paper in Photochemical and Photobiological Sciences that summarized the potential benefits of PLE in preventing damage related to sun exposure.

Among its mechanism, PLE generates reactive oxygen species (ROS) and prevents depletion of Langerhans cells induced by ultraviolet (UV) light, Dr. González explained in an interview. “At the cellular level, PLE activates tumor suppression p53, inhibits UV-induced COX-2 expression, reduces inflammation, and preventions immunosuppression,” he continued. In addition, he said PLE also prevents UV-A-induced common deletions related to mitochondrial damage and MMP1 expression induced by various UV wavelengths. 
“These molecular and cellular effects may translate into long-term inhibition of carcinogenesis including actinic keratosis,” he said, noting that all of these findings “justify the work by Pellacani and collaborators.”

Dr. Pellacani reports no potential conflicts of interest. Dr. González has a financial relationship with Cantabria Laboratories.

MILAN – Application of topical or both topical and oral polypodium leucotomos extract (PLE) was associated with significant reversal of adverse skin changes in patients with severe actinic keratoses (AKs) treated over 12 months, in a randomized, blinded study presented at the annual congress of the European Academy of Dermatology and Venereology.

At 12 months, the percentage of patients with a normal or almost normal honeycomb pattern when evaluated blindly with reflectance confocal microscopy (RCM) was about twice as great in either of the two groups that received PLE relative to those treated with topical photoprotection alone, according to Giovanni Pellacani, MD, PhD, chair of dermatology, University of Sapienza, Rome.

“In patients with severe actinic keratosis, the 12-month use of a PLE-based topical or oral photoprotection is associated with positive clinical and anatomical outcomes,” Dr. Pellacani said.

PLE, which is already commonly used in sun protection products, is derived from a South American species of fern and has been proposed for a broad array of dermatologic diseases. According to Dr. Pellacani, in vivo studies associating PLE with immune photoprotection make this agent particularly promising for severe AKs.

In this study involving two clinical research centers in Italy, 131 patients with photoaging and at least three AKs were randomized to one of three treatment arms. The control arm received topical photoprotection with an SPF of 100 or higher applied twice daily to all sun-exposed areas. The two treatment arms received the same topical photoprotection plus either a PLE-containing topical cream alone or a PLE-containing topical cream plus PLE in an oral form (240 mg) once daily

Patients were evaluated at 3 months, 6 months, and 1 year with several measures, including the Actinic Keratosis Area Score Index (AKASI) and the AK Field Assessment Scale Area (AK-FAS). They were also assessed with RCM. All clinical assessments and RCM evaluations, which assessed seven different parameters, such as honeycomb pattern, mottled pigmentation, and reticulated collagen, were performed by dermatologists blinded to the treatment assignment.

Complete data were available for 116 patients who completed all three evaluations over the 12 months of follow-up. On RCM, 50% of those receiving the oral and topical forms of PLE and 45% of those receiving topical PLE had normalization of the honeycomb pattern. These responses were significantly greater (P = .04 for both) than the 26% with normalization in the control group.

Although there were no significant differences in any of the other parameters evaluated by RCM, the improvement in the honeycomb pattern was accompanied by a 7% improvement in the AKASI score in patients taking PLE, either topically or orally and topically, while there was a 6% worsening (P < .001) among controls.

The AK-FAS score improved at 12 months by 26% in the group on oral/topical PLE and by 4% in the group on topical PLE. The score worsened by 13% among controls.

Over the course of the study, patients were permitted to take an appropriate therapy, such as imiquimod, cryotherapy, or 5-flourouracil if there was worsening of the AK-FAS score or if new lesions appeared.

On this measure, 38% of controls and 11% of those randomized to topical PLE had progressive disease versus only 2% of those randomized to take both topical and oral PLE, Dr. Pellacani reported.

The lower rate of new lesions or a start of a new drug over the course of the study in the group receiving both the topical and the oral formulations of PLE relative to those receiving topical PLE alone did not reach statistical significance, but Dr. Pellacani concluded that the addition of PLE to topical photoprotection without PLE seemed to provide a potentially clinically meaningful advantage.

Larger studies and longer term studies are needed, according to Dr. Pellacani, who noted that the substantial body of clinical studies associating PLE with benefit in a variety of dermatologic disorders has been weakened by the absence of well-designed studies that are adequately powered to guide clinical use.

Salvador González, MD, PhD, a dermatology specialist at Alcalá University, Madrid, also believes that PLE deserves further evaluation not just for photoprotection but for reinvigorating damaged skin due to its antioxidant and anti-inflammatory properties. He was the senior author of a 2020 paper in Photochemical and Photobiological Sciences that summarized the potential benefits of PLE in preventing damage related to sun exposure.

Among its mechanism, PLE generates reactive oxygen species (ROS) and prevents depletion of Langerhans cells induced by ultraviolet (UV) light, Dr. González explained in an interview. “At the cellular level, PLE activates tumor suppression p53, inhibits UV-induced COX-2 expression, reduces inflammation, and preventions immunosuppression,” he continued. In addition, he said PLE also prevents UV-A-induced common deletions related to mitochondrial damage and MMP1 expression induced by various UV wavelengths. 
“These molecular and cellular effects may translate into long-term inhibition of carcinogenesis including actinic keratosis,” he said, noting that all of these findings “justify the work by Pellacani and collaborators.”

Dr. Pellacani reports no potential conflicts of interest. Dr. González has a financial relationship with Cantabria Laboratories.

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

A version of this article first appeared on Medscape.com.

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

A version of this article first appeared on Medscape.com.

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

A version of this article first appeared on Medscape.com.

The American College of Cardiology/American Heart Association have issued a set of data standards for chest pain and acute myocardial infarction to accompany the 2021 guidelines for evaluation and diagnosis of chest pain.

In October 2021, the AHA/ACC issued a joint clinical practice guideline encouraging clinicians to use standardized risk assessments, clinical pathways, and tools to evaluate and communicate with patients who present with chest pain, as reported by this news organization.

The writing group underscored the need to reach a consensus for the definitions of chest pain. The new document standardizes related data elements for consistent reporting on chest pain syndromes.

“This is an appendix to the guidelines and a planned effort to try to harmonize and bring uniformity to the language applied,” writing committee chair H.V. “Skip” Anderson, MD, with UT Health Science Center, Houston, told this news organization.

“You want heart attack to mean the same thing in Miami Beach as in Western Pennsylvania, as in Oregon and Washington and every place in between,” Dr. Anderson explained. “You want everybody to be using the same language, so that’s what these data standards are meant to do.”

In the document, data elements are grouped into three broad categories: chest pain, myocardial injury, and MI.

“We deliberately followed the plans contained in the new guideline and focused on potentially serious cardiovascular causes of chest pain as might be encountered in emergency departments,” the writing group notes in the document.

The terms “typical” and “atypical” as descriptors of chest pain or anginal syndromes are not used in the new document, in line with the 2021 guidance to abandon these terms.

Instead, the new document divides chest pain syndromes into three categories: “cardiac,” “possible cardiac,” and “noncardiac” – again, in keeping with the chest pain guideline.

The document also includes data elements for risk stratification scoring according to several common risk scoring algorithms and for procedure-related myocardial injury and procedure-related MI.

Each year, chest pain sends more than 7 million adults to the emergency department in the United States. Although noncardiac causes of chest pain make up a large majority of these cases, there are several life-threatening causes of chest pain that must be identified and treated promptly.

Distinguishing between serious and nonserious causes of chest pain is an urgent imperative, the writing group says.

Overall, they say this new clinical lexicon and set of data standards should be “broadly applicable” in various settings, including clinical trials and observational studies, patient care, electronic health records (EHRs), quality and performance improvement initiatives, registries, and public reporting programs.

The 2022 ACC/AHA Key Data Elements and Definitions for Chest Pain and Acute Myocardial Infarction was simultaneously published online in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.

It was developed in collaboration with the American College of Emergency Physicians and the Society for Cardiac Angiography and Interventions and endorsed by the Society for Academic Emergency Medicine.

Dr. Anderson noted that “almost all of the guidelines that come out now, certainly in the last few years, have been followed after a certain interval by a set of data standards applicable to the guidelines.”

“It would be really great if it could actually be attached as an appendix, but the nature of the development of these things is such that there will always be a bit of a time lag between the writing group that develops the guidelines and the work group that develops the data standards; you can’t really have them working in parallel at the same time,” Dr. Anderson said in an interview.

This research had no commercial funding. The authors have no relevant disclosures.

A version of this article first appeared on Medscape.com.

The American College of Cardiology/American Heart Association have issued a set of data standards for chest pain and acute myocardial infarction to accompany the 2021 guidelines for evaluation and diagnosis of chest pain.

In October 2021, the AHA/ACC issued a joint clinical practice guideline encouraging clinicians to use standardized risk assessments, clinical pathways, and tools to evaluate and communicate with patients who present with chest pain, as reported by this news organization.

The writing group underscored the need to reach a consensus for the definitions of chest pain. The new document standardizes related data elements for consistent reporting on chest pain syndromes.

“This is an appendix to the guidelines and a planned effort to try to harmonize and bring uniformity to the language applied,” writing committee chair H.V. “Skip” Anderson, MD, with UT Health Science Center, Houston, told this news organization.

“You want heart attack to mean the same thing in Miami Beach as in Western Pennsylvania, as in Oregon and Washington and every place in between,” Dr. Anderson explained. “You want everybody to be using the same language, so that’s what these data standards are meant to do.”

In the document, data elements are grouped into three broad categories: chest pain, myocardial injury, and MI.

“We deliberately followed the plans contained in the new guideline and focused on potentially serious cardiovascular causes of chest pain as might be encountered in emergency departments,” the writing group notes in the document.

The terms “typical” and “atypical” as descriptors of chest pain or anginal syndromes are not used in the new document, in line with the 2021 guidance to abandon these terms.

Instead, the new document divides chest pain syndromes into three categories: “cardiac,” “possible cardiac,” and “noncardiac” – again, in keeping with the chest pain guideline.

The document also includes data elements for risk stratification scoring according to several common risk scoring algorithms and for procedure-related myocardial injury and procedure-related MI.

Each year, chest pain sends more than 7 million adults to the emergency department in the United States. Although noncardiac causes of chest pain make up a large majority of these cases, there are several life-threatening causes of chest pain that must be identified and treated promptly.

Distinguishing between serious and nonserious causes of chest pain is an urgent imperative, the writing group says.

Overall, they say this new clinical lexicon and set of data standards should be “broadly applicable” in various settings, including clinical trials and observational studies, patient care, electronic health records (EHRs), quality and performance improvement initiatives, registries, and public reporting programs.

The 2022 ACC/AHA Key Data Elements and Definitions for Chest Pain and Acute Myocardial Infarction was simultaneously published online in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.

It was developed in collaboration with the American College of Emergency Physicians and the Society for Cardiac Angiography and Interventions and endorsed by the Society for Academic Emergency Medicine.

Dr. Anderson noted that “almost all of the guidelines that come out now, certainly in the last few years, have been followed after a certain interval by a set of data standards applicable to the guidelines.”

“It would be really great if it could actually be attached as an appendix, but the nature of the development of these things is such that there will always be a bit of a time lag between the writing group that develops the guidelines and the work group that develops the data standards; you can’t really have them working in parallel at the same time,” Dr. Anderson said in an interview.

This research had no commercial funding. The authors have no relevant disclosures.

A version of this article first appeared on Medscape.com.

The American College of Cardiology/American Heart Association have issued a set of data standards for chest pain and acute myocardial infarction to accompany the 2021 guidelines for evaluation and diagnosis of chest pain.

In October 2021, the AHA/ACC issued a joint clinical practice guideline encouraging clinicians to use standardized risk assessments, clinical pathways, and tools to evaluate and communicate with patients who present with chest pain, as reported by this news organization.

The writing group underscored the need to reach a consensus for the definitions of chest pain. The new document standardizes related data elements for consistent reporting on chest pain syndromes.

“This is an appendix to the guidelines and a planned effort to try to harmonize and bring uniformity to the language applied,” writing committee chair H.V. “Skip” Anderson, MD, with UT Health Science Center, Houston, told this news organization.

“You want heart attack to mean the same thing in Miami Beach as in Western Pennsylvania, as in Oregon and Washington and every place in between,” Dr. Anderson explained. “You want everybody to be using the same language, so that’s what these data standards are meant to do.”

In the document, data elements are grouped into three broad categories: chest pain, myocardial injury, and MI.

“We deliberately followed the plans contained in the new guideline and focused on potentially serious cardiovascular causes of chest pain as might be encountered in emergency departments,” the writing group notes in the document.

The terms “typical” and “atypical” as descriptors of chest pain or anginal syndromes are not used in the new document, in line with the 2021 guidance to abandon these terms.

Instead, the new document divides chest pain syndromes into three categories: “cardiac,” “possible cardiac,” and “noncardiac” – again, in keeping with the chest pain guideline.

The document also includes data elements for risk stratification scoring according to several common risk scoring algorithms and for procedure-related myocardial injury and procedure-related MI.

Each year, chest pain sends more than 7 million adults to the emergency department in the United States. Although noncardiac causes of chest pain make up a large majority of these cases, there are several life-threatening causes of chest pain that must be identified and treated promptly.

Distinguishing between serious and nonserious causes of chest pain is an urgent imperative, the writing group says.

Overall, they say this new clinical lexicon and set of data standards should be “broadly applicable” in various settings, including clinical trials and observational studies, patient care, electronic health records (EHRs), quality and performance improvement initiatives, registries, and public reporting programs.

The 2022 ACC/AHA Key Data Elements and Definitions for Chest Pain and Acute Myocardial Infarction was simultaneously published online in the Journal of the American College of Cardiology and Circulation: Cardiovascular Quality and Outcomes.

It was developed in collaboration with the American College of Emergency Physicians and the Society for Cardiac Angiography and Interventions and endorsed by the Society for Academic Emergency Medicine.

Dr. Anderson noted that “almost all of the guidelines that come out now, certainly in the last few years, have been followed after a certain interval by a set of data standards applicable to the guidelines.”

“It would be really great if it could actually be attached as an appendix, but the nature of the development of these things is such that there will always be a bit of a time lag between the writing group that develops the guidelines and the work group that develops the data standards; you can’t really have them working in parallel at the same time,” Dr. Anderson said in an interview.

This research had no commercial funding. The authors have no relevant disclosures.

A version of this article first appeared on Medscape.com.

There’s strong evidence that training parents to guide the development of children with autism reaps consistent benefits, according to a systematic review and meta-analysis of more than 50 high-quality studies.

“Referrals for parent training should now be considered the expected standard for medical practice,” said a member of the research team, Timothy B. Smith, PhD, a professor of psychology at Brigham Young University, Provo, Utah.

Methods and results

The meta-analysis included 54 papers based on randomized clinical trials involving 2,895 children, which compared the effects of various parent interventions with professional treatment, treatment as usual, or being on a wait-list to receive an intervention.

Overall the research team reported “moderately strong” average benefits from the parent-mediated interventions (Hedges’ g, 0.553), indicating a medium effect size. Parent interventions had the greatest effect on outcomes involving positive behavior and social skills (0.603), followed by language and communication (0.545), maladaptive behavior (0.519), and life skills (0.239).

Similar benefits were observed regardless of a child’s age or sex or which parent or parents implemented an intervention. The effects also appeared to be consistent regardless of intervention characteristics, such as the number of training sessions parents received, although the researchers noted that many studies did not provide data on such details.

Paul Carbone, MD, a professor of pediatrics at the University of Utah, Salt Lake City, who was not involved in the review, said it demonstrates that such parental engagement is “vitally important” and pediatricians “should not hesitate to refer interested families.”

Overcoming limitations, future research needs

The research team attempted to overcome limitations with previous reviews by using comprehensive search terms and other methods to identify relevant studies, including some that had not been published. They included only studies that reflect common practice of training multiple parents simultaneously, they wrote.

Dr. Smith noted that long-term outcomes data and further study to compare effects on children with mild, moderate, and severe autism are needed.

Although logic would suggest greater benefits for children with severe disease, there are no data to demonstrate that, he said.

The authors of the study and Dr. Carbone reported no relevant competing interests.

There’s strong evidence that training parents to guide the development of children with autism reaps consistent benefits, according to a systematic review and meta-analysis of more than 50 high-quality studies.

“Referrals for parent training should now be considered the expected standard for medical practice,” said a member of the research team, Timothy B. Smith, PhD, a professor of psychology at Brigham Young University, Provo, Utah.

Methods and results

The meta-analysis included 54 papers based on randomized clinical trials involving 2,895 children, which compared the effects of various parent interventions with professional treatment, treatment as usual, or being on a wait-list to receive an intervention.

Overall the research team reported “moderately strong” average benefits from the parent-mediated interventions (Hedges’ g, 0.553), indicating a medium effect size. Parent interventions had the greatest effect on outcomes involving positive behavior and social skills (0.603), followed by language and communication (0.545), maladaptive behavior (0.519), and life skills (0.239).

Similar benefits were observed regardless of a child’s age or sex or which parent or parents implemented an intervention. The effects also appeared to be consistent regardless of intervention characteristics, such as the number of training sessions parents received, although the researchers noted that many studies did not provide data on such details.

Paul Carbone, MD, a professor of pediatrics at the University of Utah, Salt Lake City, who was not involved in the review, said it demonstrates that such parental engagement is “vitally important” and pediatricians “should not hesitate to refer interested families.”

Overcoming limitations, future research needs

The research team attempted to overcome limitations with previous reviews by using comprehensive search terms and other methods to identify relevant studies, including some that had not been published. They included only studies that reflect common practice of training multiple parents simultaneously, they wrote.

Dr. Smith noted that long-term outcomes data and further study to compare effects on children with mild, moderate, and severe autism are needed.

Although logic would suggest greater benefits for children with severe disease, there are no data to demonstrate that, he said.

The authors of the study and Dr. Carbone reported no relevant competing interests.

There’s strong evidence that training parents to guide the development of children with autism reaps consistent benefits, according to a systematic review and meta-analysis of more than 50 high-quality studies.

“Referrals for parent training should now be considered the expected standard for medical practice,” said a member of the research team, Timothy B. Smith, PhD, a professor of psychology at Brigham Young University, Provo, Utah.

Methods and results

The meta-analysis included 54 papers based on randomized clinical trials involving 2,895 children, which compared the effects of various parent interventions with professional treatment, treatment as usual, or being on a wait-list to receive an intervention.

Overall the research team reported “moderately strong” average benefits from the parent-mediated interventions (Hedges’ g, 0.553), indicating a medium effect size. Parent interventions had the greatest effect on outcomes involving positive behavior and social skills (0.603), followed by language and communication (0.545), maladaptive behavior (0.519), and life skills (0.239).

Similar benefits were observed regardless of a child’s age or sex or which parent or parents implemented an intervention. The effects also appeared to be consistent regardless of intervention characteristics, such as the number of training sessions parents received, although the researchers noted that many studies did not provide data on such details.

Paul Carbone, MD, a professor of pediatrics at the University of Utah, Salt Lake City, who was not involved in the review, said it demonstrates that such parental engagement is “vitally important” and pediatricians “should not hesitate to refer interested families.”

Overcoming limitations, future research needs

The research team attempted to overcome limitations with previous reviews by using comprehensive search terms and other methods to identify relevant studies, including some that had not been published. They included only studies that reflect common practice of training multiple parents simultaneously, they wrote.

Dr. Smith noted that long-term outcomes data and further study to compare effects on children with mild, moderate, and severe autism are needed.

Although logic would suggest greater benefits for children with severe disease, there are no data to demonstrate that, he said.

The authors of the study and Dr. Carbone reported no relevant competing interests.

Purpose

Examine hepatitis B virus (HBV) testing in veterans receiving systemic anticancer treatment (SACT) in the Veterans Health Administration (VHA).

Background

HBV reactivation is reported in patients with chronic (HB surface antigen, HBsAg, positive) or prior (HB core antibody, HBcAb, positive) HBV infection, who receive SACT. A recent American Society of Clinical Oncology provisional clinical opinion update recommended HBV screening for all patients prior to initiation of SACT (excluding hormonal therapy). HBV testing and the incidence of hepatitis in veterans receiving SACT in the VHA has not been reported.

Methods/Data Analysis

VHA EHR data were used to identify veterans receiving SACT (01/2010-12/2021). Testing for HBsAg, HBcAb and alanine aminotransferase (ALT) was extracted. Patients known to have HBV or elevated ALT prior to first SACT, and those receiving anti-CD20 were excluded. Patients were followed until two years after the last SACT or 12/2021, whichever occurred first. Patients receiving intravenous SACT and those receiving oral SACT are described separately.

Results

Between 2010 and 2021, 215,395 veterans received an intravenous SACT, while 80,752 veterans received an oral SACT. Of patients treated with an SACT, 80% had no evidence of HBsAg or HBcAb testing prior to treatment initiation, and 8-12% experienced at least one elevated ALT between treatment initiation and two years after the last SACT. There was no evidence of increased ALT elevation in patients who were not tested compared to those that were tested prior to treatment initiation. In patients with at least one ALT elevation, approximately 30% were tested for HBV and of these, 3% tested positive.

Conclusions/Implications

Most veterans receiving SACT are not tested for HBV prior to treatment initiation, and do not experience elevated ALTs. In patients with elevated ALT during or subsequent to SACT, the majority are not tested for HBV. Veterans that are tested reveal an HBV prevalence of about 10%. Our results suggest that HBV testing prior to SACT initiation should not be at the expense of delaying treatment, given the magnitude of proposed change from current practice and the anticipated low probability of benefit.

Purpose

Examine hepatitis B virus (HBV) testing in veterans receiving systemic anticancer treatment (SACT) in the Veterans Health Administration (VHA).

Background

HBV reactivation is reported in patients with chronic (HB surface antigen, HBsAg, positive) or prior (HB core antibody, HBcAb, positive) HBV infection, who receive SACT. A recent American Society of Clinical Oncology provisional clinical opinion update recommended HBV screening for all patients prior to initiation of SACT (excluding hormonal therapy). HBV testing and the incidence of hepatitis in veterans receiving SACT in the VHA has not been reported.

Methods/Data Analysis

VHA EHR data were used to identify veterans receiving SACT (01/2010-12/2021). Testing for HBsAg, HBcAb and alanine aminotransferase (ALT) was extracted. Patients known to have HBV or elevated ALT prior to first SACT, and those receiving anti-CD20 were excluded. Patients were followed until two years after the last SACT or 12/2021, whichever occurred first. Patients receiving intravenous SACT and those receiving oral SACT are described separately.

Results

Between 2010 and 2021, 215,395 veterans received an intravenous SACT, while 80,752 veterans received an oral SACT. Of patients treated with an SACT, 80% had no evidence of HBsAg or HBcAb testing prior to treatment initiation, and 8-12% experienced at least one elevated ALT between treatment initiation and two years after the last SACT. There was no evidence of increased ALT elevation in patients who were not tested compared to those that were tested prior to treatment initiation. In patients with at least one ALT elevation, approximately 30% were tested for HBV and of these, 3% tested positive.

Conclusions/Implications

Most veterans receiving SACT are not tested for HBV prior to treatment initiation, and do not experience elevated ALTs. In patients with elevated ALT during or subsequent to SACT, the majority are not tested for HBV. Veterans that are tested reveal an HBV prevalence of about 10%. Our results suggest that HBV testing prior to SACT initiation should not be at the expense of delaying treatment, given the magnitude of proposed change from current practice and the anticipated low probability of benefit.

Purpose

Examine hepatitis B virus (HBV) testing in veterans receiving systemic anticancer treatment (SACT) in the Veterans Health Administration (VHA).

Background

HBV reactivation is reported in patients with chronic (HB surface antigen, HBsAg, positive) or prior (HB core antibody, HBcAb, positive) HBV infection, who receive SACT. A recent American Society of Clinical Oncology provisional clinical opinion update recommended HBV screening for all patients prior to initiation of SACT (excluding hormonal therapy). HBV testing and the incidence of hepatitis in veterans receiving SACT in the VHA has not been reported.

Methods/Data Analysis

VHA EHR data were used to identify veterans receiving SACT (01/2010-12/2021). Testing for HBsAg, HBcAb and alanine aminotransferase (ALT) was extracted. Patients known to have HBV or elevated ALT prior to first SACT, and those receiving anti-CD20 were excluded. Patients were followed until two years after the last SACT or 12/2021, whichever occurred first. Patients receiving intravenous SACT and those receiving oral SACT are described separately.

Results

Between 2010 and 2021, 215,395 veterans received an intravenous SACT, while 80,752 veterans received an oral SACT. Of patients treated with an SACT, 80% had no evidence of HBsAg or HBcAb testing prior to treatment initiation, and 8-12% experienced at least one elevated ALT between treatment initiation and two years after the last SACT. There was no evidence of increased ALT elevation in patients who were not tested compared to those that were tested prior to treatment initiation. In patients with at least one ALT elevation, approximately 30% were tested for HBV and of these, 3% tested positive.

Conclusions/Implications

Most veterans receiving SACT are not tested for HBV prior to treatment initiation, and do not experience elevated ALTs. In patients with elevated ALT during or subsequent to SACT, the majority are not tested for HBV. Veterans that are tested reveal an HBV prevalence of about 10%. Our results suggest that HBV testing prior to SACT initiation should not be at the expense of delaying treatment, given the magnitude of proposed change from current practice and the anticipated low probability of benefit.

AGA is accepting applications for the third annual AGA-Aman Armaan Ahmed Family Summer Undergraduate Research Fellowship (SURF).

Eight undergraduate students from groups traditionally underrepresented in biomedical research will have the opportunity to perform 10 weeks of research related to digestive diseases alongside an established investigator. Recipients will also receive a $5,400 stipend and funding to offset travel and meal expenses.

Students may independently secure support from an AGA member mentor or choose from our list of participating mentors. Past recipients are eligible to apply!

Additional information about the award, including application requirements and a downloadable preview, are available in the request for applications. Please see important dates below.
 

• Dec. 14, 2022 - Online applications close at 11:59 p.m. ET.
• March 2023 - Applicants are notified of their status.
• May-August 2023 - Recipients perform summer research with mentors.

AGA gratefully acknowledges the Aman Armaan Ahmed Family for supporting this program.

AGA is accepting applications for the third annual AGA-Aman Armaan Ahmed Family Summer Undergraduate Research Fellowship (SURF).

Eight undergraduate students from groups traditionally underrepresented in biomedical research will have the opportunity to perform 10 weeks of research related to digestive diseases alongside an established investigator. Recipients will also receive a $5,400 stipend and funding to offset travel and meal expenses.

Students may independently secure support from an AGA member mentor or choose from our list of participating mentors. Past recipients are eligible to apply!

Additional information about the award, including application requirements and a downloadable preview, are available in the request for applications. Please see important dates below.
 

• Dec. 14, 2022 - Online applications close at 11:59 p.m. ET.
• March 2023 - Applicants are notified of their status.
• May-August 2023 - Recipients perform summer research with mentors.

AGA gratefully acknowledges the Aman Armaan Ahmed Family for supporting this program.

AGA is accepting applications for the third annual AGA-Aman Armaan Ahmed Family Summer Undergraduate Research Fellowship (SURF).

Eight undergraduate students from groups traditionally underrepresented in biomedical research will have the opportunity to perform 10 weeks of research related to digestive diseases alongside an established investigator. Recipients will also receive a $5,400 stipend and funding to offset travel and meal expenses.

Students may independently secure support from an AGA member mentor or choose from our list of participating mentors. Past recipients are eligible to apply!

Additional information about the award, including application requirements and a downloadable preview, are available in the request for applications. Please see important dates below.
 

• Dec. 14, 2022 - Online applications close at 11:59 p.m. ET.
• March 2023 - Applicants are notified of their status.
• May-August 2023 - Recipients perform summer research with mentors.

AGA gratefully acknowledges the Aman Armaan Ahmed Family for supporting this program.

Background

Diffuse large B-cell lymphoma (DLBCL) is the most common aggressive type of non- Hodgkin lymphoma (NHL), comprising 30% of all NHL. Due to a decreased state of immunosurveillance resulting from the disease itself and its associated therapies, patients are at increased risk of developing a secondary malignancy. Multiple primary malignancies have been reported to occur in up to 15% of patients with DLBCL, retrospectively.

Herein, we review a case of a man with DLBCL who concomitantly developed ALK negative anaplastic large cell lymphoma (ALCL) distinctly of T-cell lineage who was successfully treated with palliative therapy for both diagnoses despite his advanced age and diagnosis associated with a poor prognosis with continued effect and sustained quality of life.

Case Report

An 88-year-old man presented with stage III DLBCL, diagnosed in 12/2018, was deemed not to be an aggressive therapy candidate. As such, he was treated with Rituximab monotherapy for 6 cycles, ending in 02/2019, with remarkably good effect. He remained in a PR with stable disease on serial PET/CTs until 09/2021, at which time he was noted to have Horner’s Syndrome in clinic. CT chest demonstrated a right apical lung mass, not previously seen on prior scans measuring 4.2 x 2.7 cm. Other sites of nodal disease remained stable on PET/CT.

Biopsy of the lesion revealed CD30+ ALK-negative ALCL with distinct T-cell marker positivity on immunohistochemistry and the absence of B-cell lineage markers. After discussion at our treatment planning conference, we decided to treat with brentuximab-vedotin (Bv) monotherapy for 6 cycles. End of treatment PET/CT demonstrated a PR with near resolution in background PET avidity at the lesion. His symptoms of Horner syndrome also improved.

Conclusion

A diagnosis of aggressive lymphoma increases the risk of developing a secondary malignancy and providers should remain vigilant of this. Elderly individuals in whom aggressive therapies may be precluded can still greatly benefit from palliative targeted therapy even in the setting of diseases historically associated with a poor prognosis.

Background

Diffuse large B-cell lymphoma (DLBCL) is the most common aggressive type of non- Hodgkin lymphoma (NHL), comprising 30% of all NHL. Due to a decreased state of immunosurveillance resulting from the disease itself and its associated therapies, patients are at increased risk of developing a secondary malignancy. Multiple primary malignancies have been reported to occur in up to 15% of patients with DLBCL, retrospectively.

Herein, we review a case of a man with DLBCL who concomitantly developed ALK negative anaplastic large cell lymphoma (ALCL) distinctly of T-cell lineage who was successfully treated with palliative therapy for both diagnoses despite his advanced age and diagnosis associated with a poor prognosis with continued effect and sustained quality of life.

Case Report

An 88-year-old man presented with stage III DLBCL, diagnosed in 12/2018, was deemed not to be an aggressive therapy candidate. As such, he was treated with Rituximab monotherapy for 6 cycles, ending in 02/2019, with remarkably good effect. He remained in a PR with stable disease on serial PET/CTs until 09/2021, at which time he was noted to have Horner’s Syndrome in clinic. CT chest demonstrated a right apical lung mass, not previously seen on prior scans measuring 4.2 x 2.7 cm. Other sites of nodal disease remained stable on PET/CT.

Biopsy of the lesion revealed CD30+ ALK-negative ALCL with distinct T-cell marker positivity on immunohistochemistry and the absence of B-cell lineage markers. After discussion at our treatment planning conference, we decided to treat with brentuximab-vedotin (Bv) monotherapy for 6 cycles. End of treatment PET/CT demonstrated a PR with near resolution in background PET avidity at the lesion. His symptoms of Horner syndrome also improved.

Conclusion

A diagnosis of aggressive lymphoma increases the risk of developing a secondary malignancy and providers should remain vigilant of this. Elderly individuals in whom aggressive therapies may be precluded can still greatly benefit from palliative targeted therapy even in the setting of diseases historically associated with a poor prognosis.

Background

Diffuse large B-cell lymphoma (DLBCL) is the most common aggressive type of non- Hodgkin lymphoma (NHL), comprising 30% of all NHL. Due to a decreased state of immunosurveillance resulting from the disease itself and its associated therapies, patients are at increased risk of developing a secondary malignancy. Multiple primary malignancies have been reported to occur in up to 15% of patients with DLBCL, retrospectively.

Herein, we review a case of a man with DLBCL who concomitantly developed ALK negative anaplastic large cell lymphoma (ALCL) distinctly of T-cell lineage who was successfully treated with palliative therapy for both diagnoses despite his advanced age and diagnosis associated with a poor prognosis with continued effect and sustained quality of life.

Case Report

An 88-year-old man presented with stage III DLBCL, diagnosed in 12/2018, was deemed not to be an aggressive therapy candidate. As such, he was treated with Rituximab monotherapy for 6 cycles, ending in 02/2019, with remarkably good effect. He remained in a PR with stable disease on serial PET/CTs until 09/2021, at which time he was noted to have Horner’s Syndrome in clinic. CT chest demonstrated a right apical lung mass, not previously seen on prior scans measuring 4.2 x 2.7 cm. Other sites of nodal disease remained stable on PET/CT.

Biopsy of the lesion revealed CD30+ ALK-negative ALCL with distinct T-cell marker positivity on immunohistochemistry and the absence of B-cell lineage markers. After discussion at our treatment planning conference, we decided to treat with brentuximab-vedotin (Bv) monotherapy for 6 cycles. End of treatment PET/CT demonstrated a PR with near resolution in background PET avidity at the lesion. His symptoms of Horner syndrome also improved.

Conclusion

A diagnosis of aggressive lymphoma increases the risk of developing a secondary malignancy and providers should remain vigilant of this. Elderly individuals in whom aggressive therapies may be precluded can still greatly benefit from palliative targeted therapy even in the setting of diseases historically associated with a poor prognosis.

The AGA Women in GI Regional Workshops – four separate events across the U.S. beginning in October – will provide women physicians and scientists with effective and accessible career development and networking to support professional success and work-life balance.

Registration is now open for the Midwest and Northeast workshops.

Each workshop is an opportunity to gain new knowledge from a unique lineup of experts and various topics. Select attendees also have the opportunity to participate in the Women’s Leadership Collaboration Conference at AGA Headquarters (Dec. 2-3, 2022) to advance the work from the regional events nationally. To register and for more information on the regional workshops, please visit www.gastro.org/AGAWomensRegional.

The AGA Women in GI Regional Workshops – four separate events across the U.S. beginning in October – will provide women physicians and scientists with effective and accessible career development and networking to support professional success and work-life balance.

Registration is now open for the Midwest and Northeast workshops.

Each workshop is an opportunity to gain new knowledge from a unique lineup of experts and various topics. Select attendees also have the opportunity to participate in the Women’s Leadership Collaboration Conference at AGA Headquarters (Dec. 2-3, 2022) to advance the work from the regional events nationally. To register and for more information on the regional workshops, please visit www.gastro.org/AGAWomensRegional.

The AGA Women in GI Regional Workshops – four separate events across the U.S. beginning in October – will provide women physicians and scientists with effective and accessible career development and networking to support professional success and work-life balance.

Registration is now open for the Midwest and Northeast workshops.

Each workshop is an opportunity to gain new knowledge from a unique lineup of experts and various topics. Select attendees also have the opportunity to participate in the Women’s Leadership Collaboration Conference at AGA Headquarters (Dec. 2-3, 2022) to advance the work from the regional events nationally. To register and for more information on the regional workshops, please visit www.gastro.org/AGAWomensRegional.